Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Ca2+-activated myosin ATPase activity in isoproterenol-induced hypertrophied left ventricle increased by 20-30% while in Goldblatt rats hypertrophy occurred with a decreased myosin ATPase activity. In non-dissociating (pyrophosphate) gel electrophoresis isoproterenol treatment showed decreased V2 and V3 myosin isozymes; at the higher dose of isoproterenol (0.5 mg/kg body weight) only V1 was present. In contrast a shift toward the V3 isozyme is present in the ventricles of Goldblatt rats. One group of rats was treated with toxic doses of digitoxin: no hypertrophy occurred but there was a disappearance of V1 and V2 isozymes and a 50% decrease in Ca2+-activated ATPase activity. Thus low doses of isoproterenol produce hypertrophy with an isozyme pattern similar to that found in young (approximately 4-6 weeks old) rats. The results with digitoxin show that shifts in the cardiac isozyme distribution can occur without hypertrophy.
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PMID:Changes in myosin isozyme distribution induced by low doses of isoproterenol. 621 44

The distribution of cardiac myosin isoenzymes is altered as a result of pressure overload and physical training. Using polyacrylamide gel electrophoresis in sodium pyrophosphate, it was found that myosin from left ventricles of adult rats exists in three polymorphic forms, V1, V2 and V3. Cardiac hypertrophy due to renal hypertension (Goldblatt II) led to a shift of the isoenzymes towards V3, whereas swimming training resulted in an opposite redistribution. The isoenzyme V1 predominated, only traces of V2 and V3 were detectable. The changes in the isoenzyme distribution were reflected in an altered ATPase activity of myofibrils. In a representative sample of the Goldblatt rats, the activity was reduced by 11%, and the swimming training led to an increase by 10%. Changes in myofibrillar ATPase can, therefore, be traced to alterations in the isoenzyme pattern of myosin. The polymorphism of myosin has a two-faced aspect as regards cardiac performance. For example, a shift towards V3 is expected to increase the economy for tension development during isovolumetric contraction at the expense of a reduced maximum speed of ventricular contraction.
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PMID:The adaptive changes in the isoenzyme pattern of myosin from hypertrophied rat myocardium as a result of pressure overload and physical training. 645 82

Modifications to cell relaxation and handling of intracellular Ca have been demonstrated in animals with cardiac cell hypertrophy leading to decompensated heart failure. A previously described model of renal hypertension leading to cardiac cell hypertrophy in the guinea pig, produced using the Goldblatt 2-kidney, 1-clip technique, was used to investigate which of the main mechanisms causing cell relaxation (the sarcoplasmic reticulum Ca-adenosinetriphosphatase and Na/Ca exchanger) are altered in hypertrophy. Relaxation upon rewarming from a rapid cooling contracture was slowed in hypertrophied (H) compared with control (C) cells. Relaxation was further slowed in H compared with C cells when Na/Ca exchange was inhibited by rewarming in a Na-free, Ca-free solution and slowed most markedly in H cells in the presence of 10 mM caffeine. Hypertrophy led to greater modification of cell length relaxation in comparison with the decline in the indo-1 transient, but the force-pCa relationship in skinned muscles showed that myofilament sensitivity was unchanged. Such results indicate that cell relaxation and Ca handling are affected in hypertrophy, possibly involving modifications of Na/Ca exchange activity.
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PMID:Effect of hypertrophy on mechanisms of relaxation in isolated cardiac myocytes from guinea pig. 797 15

Changes in unloaded maximum shortening velocity (Vmax) and myosin isoenzymes (MI) composition of rat left ventricular muscle were examined in the 8-week or 16-week Goldblatt hypertensive (H8, H16) and hypertension-regressive rats (R8). The Vmax was estimated by extrapolation to zero afterload from the tension-velocity curve of left ventricular papillary muscle, while the MI composition (V1, V2 and V3) was separated by polyacrylamide gel electrophoresis and determined by densitometry. The results showed that: (1) A slow age-dependent shift to V3 and a decrease in Vmax were observed in 16- and 24-week-old rats (S8, S16), in which V1/V3 ratio was decreased respectively by 38.9% and 61.0% and Vmax was decreased respectively by 8.3% and 13.3% when compared with that of the 8-week-old rats (S0). (2) There was a significant decrease in V1/V3 ratio and Vmax in 8-week (H8) and 16-week (H16) hypertension induced hypertrophic left ventricular muscle as evidenced by the fact that the V1/V3 ratio decreased by 84.4% and 93.5% and Vmax decreased by 33.3% and 48.3% in H8 and H16 as compared with that of the control rats (S0). (3) There was a partial recovery in Vmax and V1/V3 ratio in (R8) group rats. (4) The Vmax was positively correlated with the level of V1 (r = 0.9215, P < 0.01) and negatively with the level of V3 (r = 0.9071, P < 0.01) as analyzed in all the six experimental groups of a total of 48 rats (S0, S8, S16, H8, H16, R8). In conclusion, a significant shift of the myosin isoenzymes towards low ATPase activity V3 might be the biochemical mechanism responsible, at least in part, for the decrease in maximum shortening velocity in the hypertrophic left ventricular muscle induced by pressure overload.
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PMID:[Changes in myosin isoenzymes composition and the maximum shortening velocity in hypertrophic left ventricular muscle of rats]. 938 1

The properties of the Na/K pump and Na,K,Cl cotransporter were studied in vascular tissue of two-kidney Goldblatt hypertensive rats. These transport systems were measured as ouabain-sensitive and bumetanide-sensitive 86Rb/K uptake in aortic rings, left ventricular muscle and soleus skeletal muscle fibers of control and hypertensive Sprague-Dawley rats. A dramatic increment in Na/K pump activity was observed in intact aortic rings from the hypertensive group. The same was true for the Na,K,Cl cotransporter. The transport parameters related to the left ventricular muscle and soleus skeletal muscle were not significantly altered in the hypertensive rats. Measurements of the catalytic isoforms of the Na+, K(+)-ATPase in the aortic rings indicated that both isoforms (alpha 1 and alpha 2) were elevated in the same proportion in the hypertensive rats. The results also indicate that the endothelium plays an important role in both transport systems: in the absence of endothelium, a much lower 86Rb/K uptake was observed than in intact aortic rings, either from control or hypertensive vascular tissue. Nevertheless, when the 86Rb/K transport activity was measured in denuded aortic rings, a significantly higher ouabain and bumetanide sensitive 86Rb/K uptake was also observed in the hypertensive rats. These data also show no alteration in the endothelium of the hypertensive rats as compared to control animals. The presence of endothelium had a more striking effect on the alpha 2 catalytic isoform activity than on the alpha 1 isoform. We conclude that there is a significant increment in the Na/K pump and Na,K,Cl cotransporter in two kidney-Goldblatt hypertension, that is specific for vascular smooth muscle.
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PMID:Increased Na,K,Cl cotransporter and Na, K-ATPase activity of vascular tissue in two-kidney Goldblatt hypertension. 983 May 14

Renin angiotensin system in the genesis of hypertension was established long after Goldblatt's belief that the minute capillaries of the kidney regulate blood pressure and he also suggested kidney released a pressure substance which lead to rise of blood pressure. Guyton provided experimental and analytical data supporting the role of renal pressure natriuresis in the regulation of normal circulation and its function resulting in the pathogenesis of hypertension. Hady and Overbeck proposed that the blood pressure of volume expanded hypertension was raised by a circulating inhibitor of the Na+/K+ ATPase pump. Brenner et al proposed that hypertension may arise from a congenital reduction in the number of nephrons or in the filtration surface area per glomerulus, thereby limiting ability to excrete sodium, raising blood pressure. Renin angiotensin system can be interrupted at four sites by adrenergic blocker, renin inhibitor, angiotensin converting enzyme inhibitor and angiotensin receptor blocker. Non-modulation in the face of relatively high dietary sodium could explain the pathogenesis of sodium sensitive hypertension and provide a more targeted, rational therapy for its correction.
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PMID:Role of kidney in hypertension. 1296 47


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